United States Pollution Prevention December 1994
Environmental and Toxics EPA 749-F-95-016a
Protection
Agency(7407)
OPPT Chemical Fact Sheets
(Phthalic Anhydride) Fact Sheet: Support Document (CAS No. 85-44-9)
This summary is based on information retrieved from a systematic search
limited to secondary sources (see Appendix A). These sources include
online databases, unpublished EPA information, government publications,
review documents, and standard reference materials. No attempt has been
made to verify information in these databases and secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical identity and physical/chemical properties of phthalic
anhydride are summarized in Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF PHTHALIC
ANHYDRIDE
Characteristic/Property Data Reference
_________________________________________________________________________
CAS No. 85-44-9
Common Synonyms 1,2-benzenedicarboxylic acid U.S. EPA anhydride; 1,3-dihydro- 1994
1,3-dioxoisobenzofurandione;
1,3-phthalandion; phthalandione
Molecular Formula C8H4O3
Chemical Structure
Physical State white solid; lustrous needles U.S. EPA 1986
Molecular Weight 148.12
Melting Point 131øC U.S. EPA 1986
Boiling Point 284øC (sublimes) Keith and
Walters 1985
Water Solubility 6.2 g/L @ 25øC U.S. EPA 1986
Density 1.527 g/mL @ 20øC Keith and
Walters 1985
Vapor Density (air = 1) 5.1 Keith and Walters 1985
KOC 36 (estimated) U.S. EPA 1986
Log KOW 1.6 (measured) Hansch and Leo 1987
Vapor Pressure 0.00052 mm Hg @ 25øC U.S. EPA 1986
Reactivity hydrolyses in water U.S. EPA 1986
Flash Point 152øC (closed cup) ACGIH 1991
Henry's Law Constant 1.6 x 10-8 atm m3/mol U.S. EPA 1986
(calculated)
Fish Bioconcentration Factor 5 (calculated) CHEMFATE 1994
Odor Threshold 0.053 ppm; air, v/v U.S. EPA 1986
Conversion Factors 1 ppm = 6.06 mg/m3 U.S. EPA 1986
1 mg/m3 = 0.165 ppm
_________________________________________________________________________
II. PRODUCTION, USE, AND TRENDS
A. Production
USITC (1994) lists seven producers of phthalic anhydride in the United
States in 1992 (see Table 3). In 1992, U.S. companies produced 896
million pounds (407 million kg) of phthalic anhydride. The U.S.
imported 53 million pounds and exported 46 million pounds of phthalic
anhydride in 1992 (Mannsville 1993).
According to Mannsville (1993), there were five US producers of
phthalic anhydride in 1993, with a combined total production capacity
of 990 million pounds. Table 2 shows U.S. phthalic anhydride
producers, plant locations, and plant capacities for 1993.
TABLE 2. U.S. PRODUCERS OF PHTHALIC ANHYDRIDE AND THEIR CAPACITIES IN
1993
Producer Location Plant Capacity
(Millions of Pounds)
________________________________________________________
Aristech (Mitsubishi) Pasadena, TX 230
Exxon Chemical Baton Rouge, LA 250
Koppers Industries Cicero, IL 165
Stepan Chemical Millsdale, IL 170
Sterling Chemical Company Texas City, TX 175
TOTAL 990
________________________________________________________
Source: Mannsville 1993.
TABLE 3. U.S. PRODUCTION AND SALES VALUE OF PHTHALIC ANHYDRIDE IN 1991
Production Sales Quantity Sales Value Average Unit Value
(1,000 Kg) (1,000 Kg) ($1,000) (Per Kg)
________________________________________________________________________
407,350 162,965 115,698 $0.71
________________________________________________________________________
Source: USITC 1994.
B. Uses
Phthalic anhydride is used principally to produce phthalate
plasticizers used to compound flexible polyvinyl chloride. Phthalic
anhydride is also used to make unsaturated polyesters that are used
to manufacture fiberglass-reinforced plastics. Companies use these
plastics to fabricate shower stalls, synthetic marble, translucent
construction panels, boats, and recreation vehicles. Companies also
use phthalic anhydride to make alkyd resins used primarily in
solvent-borne protective coatings in the paint industry. Companies
use phthalic anhydride to make halogenated anhydrides used as fire
retardants; polyester polyols for urethanes; phthalocyanine
pigments; dyes; perfumes; pharmaceuticals; tanning and curing
agents; solvents; insect repellents; and various chemical
intermediates.
TABLE 4. END USE PATTERN OF PHTHALIC ANHYDRIDE--1992 ESTIMATE
Derivative
(Typical Standard Industrial Classification (SIC) Code)1 Percent
_____________________________________________________________________
Phthalate Plasticizers
(production, SIC 2869) 53
Unsaturated Polyesters
(production, SIC 2821) 22
Alkyd Resins
(production, SIC 2821) 18
Miscellaneous
(various SICs) 7
____________________________________________________________________
Source: Mannsville 1993.
ÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄ
1 The Standard Industrial Classification (SIC) code is the statistical
classification standard for all Federal economic statistics. The code
provides a convenient way to reference economic data on industries of
interest to the researcher. SIC codes presented here are not intended to
be an exhaustive listing; rather, the codes listed should provide an
indication of where a chemical may be likely to be found in commerce.
C. Trends
The decline in production of phthalic anhydride from 1,040 million
pounds in 1988, to 935 million pounds in 1989, was a result of
product innovations, technology changes, and product downsizing such
as that occurring in the automotive industry. However, annual
output growth of phthalic anhydride is expected to recover and
increase by two to three percent per year in the future. The
production of phthalic anhydride based polyols and unsaturated
polyesters used for reinforced plastics in transportation and
construction is expected to increase three to five percent. The
long-term demand for solvents based alkyd coatings or paints, on the
other hand, will decline. In addition, use of phthalic anhydride as
an intermediate for the production of dyes and saccharin will
decline due to decreased demand for these products. The overall
demand for plasticizers will remain even, growing by GNP rates. The
demand for dioctyl phthalate, a primary plasticizer, will drop
because of stronger environmental regulations regarding the use,
handling, and disposal of the material; non-phthalate plasticizers
marketed as substitutes will also affect demand for phthalic
anhydride (Mannsville 1993).
TABLE 5. U.S. PRODUCTION AND CAPACITY OF PHTHALIC ANHYDRIDE (MILLIONS OF
POUNDS)
Year 1990 1991 1992 1993 1995
(Projected) (Projected)
_______________________________________________________
Capacity 955 975 990 990 1070
Production 938 872 896 N/A N/A
_______________________________________________________
N/A: Not available
Source: Mannsville 1993.
III. ENVIRONMENTAL FATE
A. Environmental Release
Phthalic anhydride is released to the environment from chemical
plants, mainly those that manufacture the chemical or use it in the
production of plastics and resins (U.S. EPA 1986). The major
sources of these releases are process off-gases and industrial
effluents; however, the use of catalytic oxidation now reduces the
release of pollutants in off-gases (U.S. EPA 1986). Phthalic
anhydride has been detected in arctic air at the concentration of
10 ng/m3 (however, the EPA review notes that the presence of the
anhydride could have resulted from the hydrolysis of phthalate
esters followed by dehydration in the GC injection port), and has
been identified but not quantified in U.S. drinking water and in the
volatile flavor components of baked Idaho potatoes (U.S. EPA 1986).
In 1992, environmental releases of the chemical, as reported to the
Toxic Chemical release inventory by certain types of US industries,
totaled about 756 thousand pounds, including 750 thousand to the
atmosphere, 1 thousand pounds to land, and 5 thousand pounds to
surface water (TRI92 1994).
B. Transport
No information was found for the transport of atmospheric phthalic
anhydride. However, the water solubility of the chemical suggests
that wet deposition may occur prior to its conversion to phthalic
acid, a less soluble chemical. Because vapor phase particle
adsorption usually occurs with chemicals having a vapor pressure of
ó10-7 mm Hg (U.S. EPA 1986), adsorption is not a likely vapor phase
removal mechanism for phthalic anhydride.
No information was found for the transport of phthalic anhydride in
the aquatic environment. However, the rapid hydrolysis of phthalic
anhydride to phthalic acid that occurs in aqueous media, would
preclude any significant transport of the chemical in the aquatic
environment. Its low vapor pressure and Henry's Law constant (1.6 x
10-8 atm m3/mol) indicate that the chemical will slowly volatilize
from water (U.S. EPA 1986). The chemical is soluble in water (6,200
mg/L @ 25øC) and has a low KOC (36, estimated) and therefore has a
low potential for sedimentation or adsorption to particles,
respectively.
No information was found for the transport of phthalic anhydride in
soil. In moist soil, the chemical will hydrolyze to phthalic acid
and significant leaching is not expected to occur, other than in the
case of a large spill (U.S. EPA 1994). Significant volatilization
from soil is also unlikely based on the chemical's low vapor
pressure (0.00052 mm Hg).
C. Transformation/Persistence
1. Air The rate constant for the reaction of phthalic
anhydride with OH radicals is estimated to be 5.0 x 10-13
cm3 molecule-1 sec-1 (U.S. EPA 1986). Assuming the
concentration of OH in the atmosphere to be 106 molecules
per cubic centimeter, the estimated half-life for this
reaction is 21 days (Chemfate 1994).
2. Soil No information was found regarding the fate and
transport of phthalic anhydride in the soil (U.S. EPA
1986). Based on its rapid hydrolysis in aqueous media,
the chemical is expected to hydrolyze in moist soil.
Phthalic anhydride is also expected to undergo
biodegradation in soil, as it does in water (see below)
(U.S. EPA 1986). Under aerobic soil conditions, phthalic
anhydride probably has a half-life of >14 days (U.S. EPA
1988a).
Based on the presence of phthalic anhydride in regulated
and unregulated waste streams and in contaminated soil,
groundwater, or surface water resulting from hazardous
waste mismanagement incidents, the U.S. EPA (1988b) (under
section 4 of the Toxic Substances Control Act) required
testing of phthalic anhydride for soil adsorption. The
soil adsorption isotherm test was required, in accordance
with 796.2750 (U.S. EPA 1988b). Optional biodegradation
testing was also recommended.
3. Water Hydrolysis and biodegradation are the two
processes that may significantly degrade phthalic
anhydride in water. The hydrolytic half-life for the
chemical is about 1.5 minutes (calculated, based on the
rate constant for the forward reaction in aqueous
solution, 7.9 x 10-3 sec-1 @ 25øC) (U.S. EPA 1986).
Biodegradation values, reported in U.S. EPA 1986 for
various wastewater treatment conditions are as follows:
* 44-78% mineralization in 5 days based on
theoretical biological oxygen demand (incubation
of 1-4 mg/L of phthalic anhydride with sewage as
microbial inoculum);
* ~21% degradation in 5 days using the standard
dilution method (incubation of 2 mg/L with
sewage);
* ~18% degradation using the seawater dilution
method;
* 33% degradation in 24 hours using chemical
oxygen demand removal (incubation of 9 mg/L
phthalic anhydride with activated sludge); and
* >30% degradation in 2 weeks using the Japanese
MITI test (100 mg/L phthalic anhydride incubated
with activated sludge, pH 7 @ 25øC).
In addition, phthalic acid was 50% degraded in 1.5 weeks
in the river die-away test (using water from the
Mississippi River) and phthalic anhydride was almost
completely converted to phthalic acid in a model aquatic
ecosystem (U.S. EPA 1986).
4. Biota Phthalic anhydride, having a calculated BCF
(bioconcentration factor) value of 5, is not expected to
bioaccumulate in aquatic organisms (U.S. EPA 1986).
Studies using a model ecosystem reported log BCF values of
1.28-1.90 for daphnids, mosquito larvae, pouch snail, and
mosquito fish 24-48 hours after exposure to radiolabeled
phthalic acid (U.S. EPA 1986).
Plants and animals exposed to radiolabeled di-2-ethylhexyl
phthalate (DEHP) in a microecosystem contained, but did
not accumulate to any great extent, phthalic anhydride, a
metabolite of DEHP. The initial concentrations of DEHP,
1-2 mg/L, declined to 0.001 mg/L after 28 days. The
levels of phthalic anhydride in the various species (in
mg/kg as di-2-ethylhexyl phthalate equivalents) are as
follows: Chara chara (plant), 4.46; Mentha aquatica
(plant), 3.66; Gammarus pulex (amphipod), 0.49;
Limnephilus sp. (caddisfly), 18.99; Helobdella sp.
(leech), 0.88; Dendrocoelum lacteum (flatworm), 0.21; and
Lampetra planeri (lamprey), 0.56 (U.S. EPA 1986).
IV. HEALTH EFFECTS
A. Pharmacokinetics
1. Absorption Oral toxicity data for animals, and other
human and animal data provide indirect evidence that the
phthalic anhydride or its hydrolysis product, phthalic
acid, is absorbed from the gastrointestinal tract and
lungs. No information was found concerning dermal
absorption was found. Phthalic anhydride is a skin
irritant, and skin damage is known to result in increased
absorption of chemicals (U.S. EPA 1988a).
2. Distribution Limited information was found on the
distribution of phthalic anhydride or its hydrolysis
product, phthalic acid. One study, using an exposure
route of questionable relevance to human exposure,
indicates that fetuses from CD-1 fetal mice injected
intraperitoneally with 80 mg/kg 14C-phthalic anhydride on
days 11, 12, and 13 of gestation exhibited covalently
bound radioactivity in all tissues (U.S. EPA 1986).
3. Metabolism Phthalic anhydride is expected to undergo
hydrolysis to phthalic acid in the aqueous media of the
body (U.S. EPA 1988a). No information on the metabolism
of phthalic anhydride was found in the secondary sources
searched.
4. Excretion Humans exposed to phthalic anhydride in
workplace air excreted phthalic acid in the urine as free
acid (U.S. EPA 1988a).
B. Acute Effects
Acute exposure to phthalic anhydride produces irritation of the
eyes, skin and respiratory tract and lung sensitization in
humans. Phthalic anhydride casues sensitization in animals as
well.
1. Humans The acute toxicity of phthalic anhydride is
characterized by irritation of the eyes and skin, allergic
rhinitis, and asthma (U.S. EPA 1988a).
2. Animals LD50 values for phthalic anhydride administered
orally to animals are 800 to 1600 mg/kg for rats and 2210
mg/kg for mice (ACGIH 1991). Guinea pigs were sensitized
to 0.1% phthalic anhydride following both intracutaneous
and inhalation exposure (U.S. EPA 1986).
C. Subchronic/Chronic Effects
Workers exposed to moderate to high concentrations of
atmospheric phthalic anhydride have experienced irritation of
the eyes, skin, and respiratory tract, and have developed
hypersensitivity, bronchial asthma, and emphysema. Animals
exposed chronically to high concentrations of phthalic
anhydride in the diet exhibited lung, kidney, and adrenal gland
toxicity. EPA has derived a chronic reference dose of 2
mg/kg/day for phthalic anhydride.
1. Humans Workers exposed to atmospheric phthalic
anhydride powder at levels of ~24.9 to 77.3 ppm (21 to 67
mg/kg/day) experienced higher incidences of irritation of
the eye and respiratory tract than workers exposed to ó1.1
ppm. Irritation of the skin has also been reported in
workers (U.S. EPA 1986). Case studies document the
induction of hypersensitivity and bronchial asthma in
humans exposed to phthalic anhydride dust; specific
antibody binding against the compound has been reported
(U.S. EPA 1986). Workers currently or formerly employed
in plants producing alkyd and/or polyunsaturated resins
were evaluated for respiratory ailments (ACGIH 1991).
Time-weighted-average breathing zone samples measured 3 to
13 mg/m3 in areas where bags containing flaked phthalic
anhydride were cut open and emptied manually into reactors
several times a day during a 10- to 30-minute period. Of
the 118 individuals examined, 24% had rhinitis, 11% had
productive bronchitis, and 18% had work-associated asthma.
The latent period for the symptoms ranged from 1 to 16
years (ACGIH 1991).
Workers exposed to mixtures of phthalic anhydride and
phthalic acid developed conjunctivitis, bloody nasal
discharge, atrophy of the nasal mucosa, hoarseness, cough,
occasional bloody sputum, bronchitis, and emphysema (ACGIH
1991). Air concentrations of 30 mg/m3 (5 ppm) and 25
mg/m3 (4 ppm) were associated with conjunctivitis and
mucous membrane irritation, respectively.
2. Animals In an NCI bioassay, male and female F344 rats
and B6C3F1 mice were treated with dietary phthalic
anhydride for 105 and 104 weeks, respectively
(50/sex/group, treated; 20/sex/group, controls) (NCI
1979). The rats were exposed to 0, 7,500 or 15,000 ppm
(375 or 750 mg/kg/day). The mice were exposed to 0,
25,000, or 50,000 ppm for 32 weeks; however, these
concentrations were reduced to 12,500 and 25,000 ppm for
the males and 6,250 or 12,500 ppm for the females for the
remainder of the study because of severe weight loss. The
time-weighted-average doses were 16,346 or 32,692 ppm
(2,215 or 4,250 mg/kg/day) for the male mice and 12,019
and 24,038 ppm (1,562 or 3,125 mg/kg/day) for the female
mice. Treatment did not affect the survival of either
species and did not induce non-neoplastic gross or
microscopic pathology in the rats (see section IV.D. for
neoplastic effects).
At the end of the study, the mice exhibited weight loss
(12 and 25% for low- and high-dose males, respectively;
and 12 and 27% for low- and high-dose females,
respectively), along with significantly increased
incidences of lung and kidney lymphocytosis (both doses,
males and females), chronic bile duct inflammation (high-dose males and females), dose-related adrenal atrophy
(low- and high-dose males)(U.S.EPA 1994). Based on these
findings, the EPA identified the Lowest observed adverse
effect (LOAEL of 12,019 ppm for the female mice of the
study (U.S. EPA 1994). Using a factor of 0.13 kg food/kg
body weight to convert the dose to 1562 mg/kg/day, and
dividing by an uncertainty factor of 1000, the EPA
calculated the chronic oral RfD (reference dose) to be 2
mg/kg/day for phthalic anhydride.
In a range-finding study for the NCI bioassay, groups of 5
rats and 5 mice per sex received up to 50,000 ppm dietary
phthalic anhydride for 7 weeks (U.S. EPA 1986). Male and
female rats given 50,000 ppm exhibited a ~25% weight loss
and males given 25,000 ppm had slight centrilobular
vacuolation in the liver. There were no other lesions in
the rats and none in the mice.
Cats exposed by inhalation for seven days to 3,700 mg/m3
(611 ppm) phthalic anhydride exhibited liver and kidney
effects (U.S. EPA 1988a).
D. Carcinogenicity
No information was found for the carcinogenicity of phthalic
anhydride in humans. Phthalic anhydride was not carcinogenic
in a lifetime dietary study in mice and rats.
1. Humans No information was found in the secondary sources
searched for the carcinogenicity of phthalic anhydride in
humans.
2. Animals In an NCI bioassay, male and female F344 rats
and B6C3F1 mice were treated with dietary phthalic
anhydride for 105 and 104 weeks, respectively
(50/sex/group, treated; 20/sex/group, controls) (NCI
1979). The rats were exposed to 0, 7,500 or 15,000 ppm.
The mice were exposed to a time-weighted average
concentration of 16,346 or 32,692 ppm (see section IV.C
for further details of exposure). There were no
treatment-related effects on survival of either species
and no increased tumor incidences in male rats or male and
female mice. The female rats showed increases in
alveolar/bronchiolar adenoma (0/20, controls; 0/50, low
dose; 5/50, high dose) and in lymphomas (1/20, controls;
11/50, low dose; 4/50, high dose). However, the
interpretation of the results of the study was complicated
by nonsignificant results for lung tumors using the Fisher
exact test and an occasionally elevated spontaneous
incidence of lymphomas in historical controls. The NCI
concluded that the evidence for an association between
exposure to phthalic anhydride and the occurrence of these
tumors was questionable, and that phthalic anhydride was
not carcinogenic for F344 rats and B6C3F1 mice under the
conditions of this study.
E. Genotoxicity
Phthalic anhydride was non-mutagenic in Salmonella typhimurium
strains TA98, TA100, TA1535 and TA1537, with and without metabolic
activation, at concentrations of 3 æmol/plate in the spot test and
at concentrations of 1 to 666 æg/plate in the plate incorporation
test (U.S. EPA 1986). Phthalic anhydride was also negative in a
Salmonella reverse mutation assay and in chromosomal aberration and
sister chromatid exchange assays (U.S. EPA 1986).
F. Developmental/Reproductive Toxicity
Information on potential developmental and reproductive effects
of phthalic anhydride in humans and in animals is limited and
is not sufficient to support conclusions on these effects.
Workers exposed to phthalic anhydride have reported sexual
dysfunction.
1. Humans No information was found in the secondary sources
searched to indicate that phthalic anhydride causes
developmental toxicity in humans. A report of sexual
dysfunction among workers engaged in the manufacture of
phthalic anhydride prompted the male reproductive toxicity
study described below (an abstract from a Russian study
cited in U.S. EPA 1988a).
2. Animals Information on possible developmental effects of
phthalic anhydride is limited to several intraperitoneal
studies in animals. I.p. injection of phthalic anhydride
has produced developmental toxicity (mainly
dysmorphogenesis) in mice. In one study, injection of CD-1 mice with a minimum of 55.5 mg/kg phthalic anhydride on
gestation days 11, 12, and 13 produced "fetal
abnormalities", whereas in another, injection of 80 mg/kg
on gestation days 8, 9, and 10 produced rib and vertebral
malformations in 25.6% of the fetuses (U.S. EPA 1986). In
addition, cleft palate was also reported in fetuses
treated on days 11-13, but doses were not specified (U.S.
EPA 1986). Information on the developmental toxicity of
phthalic anhydride administered by other routes of
exposure was not found in the secondary sources searched.
An abstract from the Russian literature reports that
phthalic anhydride, administered continuously to male rats
for 45 days at concentrations of 0.2 or 1 mg/m3, decreased
the levels of ascorbic, dehydroascorbic, and/or nucleic
acids in the seminiferous tubules (U.S. EPA 1988a). No
effects were reported for the lowest concentration
administered, 0.02 mg/m3. Exposures were 24 hours/day for
45 days. Following a 2-week recovery period, the motility
of spermatozoa was one-half to one-third that of controls
for high- and mid-dose animals, respectively (U.S. EPA
1988a).
The NCI (1979) chronic dietary studies did not demonstrate
testicular effects in rodents.
G. Neurotoxicity
Information is insufficient to characterize the neurotoxicity
of phthalic anhydride in humans. Cats exposed to high
concentrations of the chemical in air exhibited loss of
appetite and drowsiness. Mice exposed to high concentrations
of phthalic anhydride in their diet exhibited mineralization of
the thalamus.
1. Humans Six workers employed for an average of 6.6 years
in a phthalic anhydride plant exhibited normal
neuromuscular activity, with the exception of one worker
who experienced a bilateral Achilles hyporeflexia (U.S.
EPA 1986).
2. Animals In a 2-year dietary study (see Section IV.C for
details about the study), mice exhibited mineralization of
the thalamus (both doses, males) (U.S.EPA 1994).
Cats exposed by inhalation for seven days to 3,700 mg/m3
(611 ppm) phthalic anhydride exhibited loss of appetite
and drowsiness (U.S. EPA 1988a).
V. ENVIRONMENTAL EFFECTS
Studies with phthalic acid, the hydrolysis product of phthalic
anhydride, suggest that the chemical is toxic to aquatic organisms
only at moderate to high concentrations. Experimental studies
suggest that phthalic anhydride is of low acute toxicity to
terrestrial animals.
A. Toxicity to Aquatic Organisms
The 96-hour LC50 for phthalic anhydride in the fathead minnow
(Pimephales promelas) is >50 mg/L (U.S. EPA 1986). Sea
lampreys (Petromyzon marinus) were not adversely affected by
exposure to 5 mg/L for 24 hours (U.S. EPA 1986). No-effect
concentrations (NOECs) reported for the hydrolysis product of
phthalic anhydride, phthalic acid, in various species are as
follows: 640 mg/L for daphnids (48 hour); 56 mg/L for fathead
minnows ("acute"); 40 mg/L for Japanese frogs (24 hours); and 5
mg/L for rainbow trout (Salmo gairdneri) and bluegill sunfish
(Lepomis macrochirus) (24 hours) (U.S. EPA 1988a).
B. Toxicity to Terrestrial Organisms
No information was found in the available literature for the
toxicity of phthalic anhydride to terrestrial organisms. The
LD50 values of 800 to 1600 mg/kg for rats and 2210 mg/kg for
mice (ACGIH 1991) suggest that the chemical would not be
acutely toxic to terrestrial animals unless present in very
high concentrations. Acute and chronic toxicity to terrestrial
plants is expected to be low (U.S. EPA 1988a).
C. Abiotic Effects
No information was found in the secondary sources searched on
the abiotic effects of phthalic anhydride.
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
The Clean Air Act Amendments of 1990 list phthalic anhydride as a
hazardous air pollutant. Occupational exposure to phthalic
anhydride is regulated by the Occupational Safety and Health
Administration (OSHA). The OSHA permissible exposure limit (PEL) is
2 parts per million of air (ppm) as an 8-hour time-weighted average
(TWA) (29 CFR 1910.000). In addition to OSHA, other federal
agencies and groups may develop recommendations to assist in
controlling workplace exposure. These agencies and groups (listed
in Tables 6 and 7) should be contacted regarding workplace exposures
and for additional information on phthalic anhydride.
TABLE 6. EPA OFFICES AND CONTACT NUMBERS INFORMATION ON PHTHALIC
ANHYDRIDE
EPA Office Statute Contact Number
_____________________________________________________________________
Pollution Prevention & Toxics PPAa (202) 260-1023
EPCRA (313/TRI)b (800) 424-9346
TSCA (4 and 12b)c (202) 554-1404
Air Clean Air Act (111 and 112B)d (919) 541-0888
Solid Waste & RCRA (Action levels: (800) 424-9346
7 mg/L, water;
200 g/kg, soil)e
Emergency Response CERCLA (RQ: 5000 lbs)f (800) 424-9346
_____________________________________________________________________
aPPA: Pollution Prevention Act
bEPCRA: Emergency Planning and Community Right to Know Act of 1986
cTSCA: Toxic Substances Control Act
dListed as hazardous air pollutant under 111 and 112B of Clean Air Act
[42 U.S.C. 7401 et seq.]
eRCRA: Resource Conservation and Recovery Act (40 CFR 264.94). Action
Level: Health and environmental-based levels used by the EPA as
indicators for the protection of human health and the environment and as
triggers for a Corrective Measure Study.
fCERCLA: Comprehensive Environmental Response, Compensation, and
Liability Act of 1980, as amended; RQ: level of hazardous substance,
which, if equaled or exceeded in a spill or release, necessitates the
immediate reporting of that release to the National Response Center (40
CFR Part 302).
TABLE 7. OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION ON
PHTHALIC ANHYDRIDE
Other Agency/Department/Group Contact Number
_________________________________________________________________________
American Conference of Governmental Industrial (513) 742-2020
Hygienists (TLV-TWA, 1 ppm)a
Consumer Product Safety Commission (301) 504-0994
Food & Drug Administration (301) 443-3170
National Institute for Occupational Safety & (800) 356-4674
Health (TWA, 1 ppm; IDLH, 1650 ppm)b
Occupational Safety & Health Administration
(TWA: 2 ppm)c
(Check local phone book under Department of Labor)
_________________________________________________________________________
aTLV-TWA: Time-weighted-average concentration for a normal 8-hour workday
and a 40-hour workweek to which nearly all workers may be repeatedly
exposed without adverse effects (ACGIH 1993-1994).
bTWA: Time-weighted-average concentrations for up to a 10-hour workday
during a 40-hour workweek. IDLH: Immediate danger to life and health.
cTWA: Time-weighted-average that must not be exceeded during any 8-hour
work shift of a 40-hour workweek. Standard promulgated pursuant to the
Occupational Safety and Health Act, 29 CFR 1910 (OSHA 1993).VI. CITED REFERENCES
ACGIH. 1991. American Conference of Governmental Industrial Hygienists,
Inc. Documentation of the Threshold Limit Values and Biological Exposure
Indices, 6th ed. ACGIH, Cincinnati, OH, pp. 1263-1265.
ACGIH. 1993-1994. Threshold Limit Values for Chemical Substances and
Physical Agents and Biological Exposure Indices. ACGIH, Cincinnati, OH,
p. 29.
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